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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

View in Context

eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–20. Life cycle of Schistosoma. Eggs are eliminated with feces or urine . Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts . The stages in the snail include two generations of sporocysts and the production of cercariae . Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host , and shed their forked tail, becoming schistosomulae . The schistosomulae migrate through several tissues and stages to their residence in the veins , ). Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species . For instance, Schistosoma japonicum is more frequently found in the superior mesenteric veins draining the small intestine , and Schistosoma mansoni occurs more often in the superior mesenteric veins draining the large intestine . However, both species can occupy either location, and they are capable of moving between sites, so it is not possible to state unequivocally that one species only occurs in one location. Schistosoma haematobium most often occurs in the venous plexus of bladder , but it can also be found in the rectal venules. The females (size 7–20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S mansoni and S japonicum) and of the bladder and ureters (S haematobium), and are eliminated with feces or urine, respectively . Pathology of S mansoni and S japonicum schistosomiasis includes Katayama fever, hepatic perisinusoidal egg granulomas, Symmers pipe stem periportal fibrosis, portal hypertension, and occasional embolic egg granulomas in brain or spinal cord. Pathology of S haematobium schistosomiasis includes hematuria, scarring, calcification, squamous cell carcinoma, and occasional embolic egg granulomas in brain or spinal cord. Human contact with water is thus necessary for infection by schistosomes. Various animals, such as dogs, cats, rodents, pigs, horse and goats, serve as reservoirs for S japonicum, and dogs for Schistosoma mekongi. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Schistomia species.

Current Medical Diagnosis & Treatment 2024 > Schistosomiasis (Bilharziasis)

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–30. Life cycle of Echinococcus. The adult Echinococcus granulosus (3–6 mm long) resides in the small bowel of the definitive hosts, dogs, or other canids. Gravid proglottids release eggs that are passed in the feces. After ingestion by a suitable intermediate host (under natural conditions: sheep, goat, swine, cattle, horses, camel), the egg hatches in the small bowel and releases an oncosphere that penetrates the intestinal wall and migrates through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a cyst that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices evaginate, attach to the intestinal mucosa , and develop into adult stages in 32–80 days. The same life cycle occurs with Echinococcus multilocularis (1.2–3.7 mm), with the following differences: the definitive hosts are foxes, and to a lesser extent dogs, cats, coyotes, and wolves; the intermediate host are small rodents; and larval growth (in the liver) remains indefinitely in the proliferative stage, resulting in invasion of the surrounding tissues. With Echinococcus vogeli (up to 5.6 mm long), the definitive hosts are bush dogs and dogs; the intermediate hosts are rodents; and the larval stage (in the liver, lungs and other organs) develops both externally and internally, resulting in multiple vesicles. Echinococcus oligarthrus (up to 2.9 mm long) has a life cycle that involves wild felids as definitive hosts and rodents as intermediate hosts. Humans become infected by ingesting eggs , with resulting release of oncospheres in the intestine and the development of cysts , , , , , in various organs. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of cystic echinococcosis.

Current Medical Diagnosis & Treatment 2024 > Invasive Cestode Infections

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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eFigure 37–43. Life cycle of Trichinella spiralis (trichina worm). Depending on the classification used, there are several species of Trichinella: T spiralis, T pseudospiralis, T nativa, T murelli, T nelsoni, T britovi, T papuae, and T zimbabwensis, all but the last of which have been implicated in human disease. Adult worms and encysted larvae develop within a single vertebrate host, and an infected animal serves as a definitive host and potential intermediate host. A second host is required to perpetuate the life cycle of Trichinella. The domestic cycle most often involves pigs and anthropophilic rodents, but other domestic animals such as horses can be involved. In the sylvatic cycle, the range of infected animals is great, but animals most often associated as sources of human infection are bear, moose, and wild boar. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae (except for T pseudospiralis and T papuae, which do not encyst) of Trichinella species . After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms . Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about 4 weeks. After 1 week, the females release larvae that migrate to striated muscles where they encyst . Diagnosis is usually made based on clinical symptoms and is confirmed by serology or identification of encysted or nonencysted larvae in biopsy or autopsy specimens. (From Global Health, Division of Parasitic Diseases and Malaria, CDC.) A flowchart of the life cycle of Trichinella spiralis, or trichina worm.

Current Medical Diagnosis & Treatment 2024 > Trichinosis

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